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. 1995 May;27(1):85-96.
doi: 10.1002/neu.480270109.

Initial sex differences in neuron growth and survival within an avian song nucleus develop in the absence of afferent input

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Initial sex differences in neuron growth and survival within an avian song nucleus develop in the absence of afferent input

M J Burek et al. J Neurobiol. 1995 May.

Abstract

Only male zebra finches (Poephila guttata) sing, and nuclei implicated in song behavior exhibit marked sex differences in neuron number. In the robust nucleus of the anterior neostriatum (RA), these sex differences develop because more neurons die in young females than in males. However, it is not known whether the sexually dimorphic survival of RA neurons is a primary event in sexual differentiation or a secondary response to sex differences in the number of cells interacting trophically with RA neurons. In particular, since sexual differentiation of the RA parallels the development of dimorphisms in the numbers of neurons providing afferent input from the lateral magnocellular nucleus of the anterior neostriatum (IMAN) and the high vocal center (HVC), it has been hypothesized that sex differences in the size of these afferent populations trigger differential RA neuron survival and growth. To test this hypothesis, we lesioned either the IMAN or both the IMAN and HVC unilaterally in 12-day-old male and female zebra finches. Subsequently, RA cell death and RA neuron number and size were measured. Unilateral IMAN lesions increased cell death and decreased neuron number and size within the ipsilateral RA of both sexes. However, even in the IMAN-lesioned hemisphere, these effects were less pronounced in males than in females, so that by day 25 the volume, number, and size of neurons were sexually dimorphic in both the contralateral and ipsilateral RA. Similarly, the absence of both IMAN and HVC afferents did not prevent the emergence of sex differences in the number and size of RA neurons by 25 days posthatching. We conclude that these sex differences within the RA are not a secondary response to dimorphisms in the numbers of IMAN or HVC neurons providing afferent input.

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